1 What is the significance of hypertension to the general patient population?

The prevalence of hypertension (HTN) is about 20% to 25% of the general population, making it a common preoperative comorbidity. It is a leading cause of death and disability in most Western societies. Long-standing HTN leads to atherosclerosis and chronic organ failure. It is a major risk factor for cardiac, vascular, cerebral, and renal disease.

2 What blood pressure value is considered hypertensive?

The numbers are somewhat arbitrary. Blood pressure (BP) changes throughout the day and can be affected by posture, exercise, medications, smoking, caffeine ingestion, and mood. HTN cannot be diagnosed on the basis of one abnormal BP reading but requires sustained elevations over multiple measurements on different days. Systemic hypertension is usually considered sustained elevations of diastolic BP greater than 90 to 95 mm Hg or a systolic BP greater than 140 to 160 mm Hg. Borderline HTN is defined as diastolic BP between 85 and 89 mm Hg or a systolic BP between 140 and 159 mm Hg. Diastolic pressures between 110 and 115 mm Hg define severe HTN, and malignant HTN is defined by BPs greater than 200/140mm Hg. Malignant HTN is a medical emergency.

3 What causes hypertension?

Essential (or idiopathic) HTN: Unknown cause; >90% of all cases fall into this category.

Endocrine: Cushing’s syndrome, hyperaldosteronism, pheochromocytoma, thyrotoxicosis, acromegaly, estrogen therapy

Renal: Chronic pyelonephritis, renovascular stenosis, glomerulonephritis, polycystic kidney disease

Neurogenic: Increased intracranial pressure, autonomic hyperreflexia

Miscellaneous: Obesity, hypercalcemia, preeclampsia, acute intermittent porphyria

4 What are some of the physiologic processes that occur as a patient becomes hypertensive?

Often cardiac output temporarily increases, followed by sustained increases in systemic vascular resistance. Vascular smooth muscular hypertrophy is observed, and there is increased arteriolar tone. Extracellular fluid volume and renin activity have no consistent pattern, but usually intracellular sodium and calcium concentrations increase. Sustained HTN leads to concentric hypertrophy of the left ventricle and impaired ventricular relaxation, known as diastolic dysfunction. Diastolic dysfunction leads to increased end-diastolic pressures.

5 Identify current drug therapies for hypertensive patients

Single-agent therapy is usually initiated; if this is ineffective, multiple agents may be prescribed. Multiple factors determine which agents are used, including race, gender, age, and comorbidities. For instance, black patients respond better to calcium channel blockers, angiotensin-converting enzyme (ACE) inhibitors, and β-blockers. β-Blockers are relatively contraindicated in patients with reactive airway disease, and patients with renal artery stenosis should not receive ACE inhibitors. Diuretics produce hypokalemia and hyperglycemia. β-Blockers are not particularly effective in elderly patients. Table 28-1 reviews commonly prescribed antihypertensive medications.

TABLE 28-1 Commonly Prescribed Antihypertensive Medications

ACE, Angiotensin-converting enzyme; MAC, minimal alveolar concentration.

Adapted from Morgan GE, Mikhail MS, Murray MJ: Clinical anesthesiology, ed 4, New York, 2005, McGraw-Hill, Chapter 20.

6 What are the consequences of sustained hypertension?

Untreated hypertensive patients develop end-organ disease, including left ventricular hypertrophy, coronary artery disease, congestive heart failure, cardiomyopathy, renal failure, and cerebrovascular accidents. Hypertensive patients also demonstrate labile BPs intraoperatively.

7 Why should antihypertensives be taken up until the time of surgery?

A well-controlled hypertensive patient has less intraoperative lability in BP. Acute withdrawal of antihypertensives may precipitate rebound HTN or myocardial ischemia. In particular, β-blockers and α₂-agonists are associated with rebound hypertension. In general antihypertensive therapy should be maintained until the time of surgery and restarted as soon as possible after surgery.

8 Which antihypertensives should be held the day of surgery?

Although there is no universal agreement, many believe ACE inhibitors and angiotensin receptor antagonists should be held the day of surgery (see Question 15). Diuretics may be withheld when depletion of intravascular volume is a concern.

9 Is regional anesthesia a viable option for hypertensive patients?

Yes, but a high level of sympathetic blockade in hypertensive patients may produce excessive reductions in BP because decreased intravascular fluid volume exacerbates vasodilation. These patients should have intravascular fluids given before the regional anesthetic.

10 Provide a differential diagnosis for intraoperative hypertension

See Table 28-2.

TABLE 28-2 Differential Diagnosis of Intraoperative Hypertension

11 How should intraoperative and postoperative hypertension be managed?

Pain is the most common cause of postoperative hypertension, but other causes should always be considered. Intraoperatively consider increasing the delivered concentration of volatile anesthetic or administering additional opioids. Consider the usual hourly doses of common opioids and determine whether the maximum limit has been reached. The usual guidelines for opioid administration may not apply to patients receiving opioids chronically. If administration of volatile agents and opioids does not address HTN sufficiently, consider primary antihypertensive agents.

After surgery opioid therapy should be titrated to respiratory rate and the patient’s interpretation of the severity of pain. Nerve blocks and analgesic adjuvants such as ketorolac should be considered. Frequently used antihypertensive agents in the perioperative period are discussed in Table 28-3.

TABLE 28-3 Antihypertensive Agents used Perioperatively

12 Are hypertensive patients undergoing general anesthesia at increased risk for perioperative cardiac morbidity?

Although numerous studies have demonstrated that increased preoperative systolic BP is a significant predictor of postoperative morbidity, there are no data that establish definitively whether the preoperative treatment of hypertension reduces perioperative risk. However, poorly treated hypertensive patients have increased intraoperative BP lability, and hemodynamic fluctuations do have some relationship to postoperative complications. In addition, some patients with hypertension will have end-organ damage. It seems reasonable that for nonemergent surgical procedures hypertension should be treated before surgery.

13 Broadly categorize the causes of perioperative hypotension

Hypovolemia: Dehydration, inadequate oral intake or preoperative intravenous fluid administration, bowel cathartics (“preps”), fever, diarrhea, vomiting

Functional hypovolemia (shock states):

Sepsis: decreased systemic vascular resistance, increased venous capacitance

Cardiac failure: ischemic heart disease, cardiomyopathy, pulmonary embolus, valvular disease, dysrhythmia

Hemorrhage: trauma, surgical blood loss, “third-spacing”

Neurogenic: loss of systemic vascular resistance from spinal cord injury

Anaphylaxis: Acute loss of systemic vascular resistance

Drugs: Including anesthetic induction agents, volatile anesthetics, histamine-releasing medications, butyrophenones, medications used to induce hypotension (e.g., ganglionic blockers, vasodilators, α- and β-adrenergic blockers), regional anesthetics

Positive-pressure ventilation

Cardiac tamponade, tension pneumothorax

Autonomic neuropathy: Diabetes mellitus, spinal cord injuries, Guillan-Barré syndrome, familiar dysautonomia, Shy-Drager syndrome, human immunodeficiency virus, or acquired immunodeficiency syndrome. Orthostatic hypotension is discussed in Chapter 1.

Medical and surgical disease: Hematemesis, melena, diabetic ketoacidosis, diabetes insipidus, high-output renal failure, bowel disease, burns

14 What is joint cement and how does it cause hypotension?

Methylmethacrylate, a cement used in joint replacement, undergoes an exothermic reaction that causes it to adhere to imperfections in the bony surface. Hypotension usually occurs 30 to 60 seconds after placement of the cement but can occur up to 10 minutes later. Postulated mechanisms include tissue damage from the reaction, release of vasoactive substances when it is hydrolyzed to methacrylate acid, embolization, and vasodilation caused by absorption of the volatile monomer.

15 Why does administration of renin-angiotensin system antagonists result in hypotension in the peri-induction period? How might the hypotension be treated?

The mechanism is believed to be loss of sympathetic tone superimposed on renin-angiotensin system (RAS) blockade. The vasopressin system is the only intact system left to maintain BP, and vasopressin release is not a fast-response system compared to the sympathetic nervous system. Administration of intravenous fluids is a proper first response. The usual pressor agents used in the operating room (phenylephrine and ephedrine) may prove insufficient if administered because of the blockade of the RAS system and the loss of sympathetic tone associated with anesthetic induction. Preparations of vasopressin have been used to correct refractory hypotension.

16 How does regional anesthesia create hypotension?

Both spinal and epidural anesthesia produce hypotension through sympathetic blockade and vasodilation, although the effects of spinal anesthesia may be more precipitous. Blocks lower than the fifth thoracic dermatome have less hypotension because of compensatory vasoconstriction of the upper extremities. Blocks higher than the fourth thoracic dermatome may affect cardioaccelerator nerves, resulting in bradycardia and diminished cardiac output (see Chapters 65 and 66).

17 How is intraoperative hypotension evaluated and treated?

Precipitous hypotension understandably requires quick treatment before all facts are at hand. Administration of adrenergic agonists and fluids is recommended. Decrease volatile or intravenous anesthetic levels. If hypotension is gradual and progressive, more facts can be taken into consideration as to the cause, but hypovolemia is the likely candidate. The effects of surgery, anesthesia, and coexisting disease are dynamic; and any single piece of information may be misleading. Thus always take into consideration as many variables as can be obtained. In addition, heart rate, BP, urine output, hematocrit, base deficit, serum lactate concentration, and response to fluid administration are valuable estimators of the cause of hypotension. Refractory hypotension requires invasive monitoring to obtain additional information about cardiac filling pressures and function.

18 Review the standard adrenergic agonists used to manage hypotension during anesthesia

The most common agents are phenylephrine and ephedrine. Their use is described in Chapter 1. Other inotropes and chronotropes are discussed in Chapter 15.

19 How should hypotension caused by cardiac ischemia be treated?

Considerations include the following:

Reducing ischemia by increasing delivered oxygen, decreasing heart rate, and coronary vasodilation with nitroglycerin

Reducing cardiac afterload (sodium nitroprusside is an arterial dilator)

Increasing contractility, using inotropes such as dopamine, dobutamine, and amrinone

Should these fail, perhaps thrombolytic therapy should be considered in concert with a cardiology consultation